The invention generally relates to cardiac pacing techniques and in particular to techniques for preventing a sudden drop in heart rate as may be caused by vasovagal syncope or other disorders.
Syncope is a sudden loss of strength or consciousness caused by reduced cerebral circulation, itself typically the result of vasodilation. Vasovagal syncope is a type of syncope referred to as a neurocardiogenic syncope wherein the syncope is triggered by an interaction between the heart and nerve tissue connected to the heart. Neurocardiogenic syncope may also be referred to as neuromediated syncope, neurally mediated syncope, cardioneurogenic syncope, vasodepressor syncope, malignant vasovagal syndrome, neurally mediated hypotension/bradycardia and cardiovascular neurogenic syncope. For vasovagal syncope, the interaction occurs between the heart and the vagus nerve.
Evidence suggests that vasovagal syncope is initially triggered by a sudden reduction in peripheral vascular resistance, perhaps resulting from stress, pooling of blood in the extremities, or other factors. As a result of the reduction in peripheral vascular resistance, the pressure of blood entering the heart drops and the amount of blood filling the ventricles prior to ventricular contractions therefore also drops. With less blood in the ventricles, the ventricles thereby contract much more quickly and vigorously than would otherwise occur in an effort to maintain a constant stroke volume. The more vigorous ventricular contractions have the effect of stimulating ventricular mechanoreceptors, also known as C fibers, that normally only respond to ventricular expansion or stretching, rather than contraction. The activation of the ventricular mechanoreceptors results in a surge in neural traffic to the brainstem, particularly to the nucleus tractus solitaries, via the vasovagal nerve.
For most people, the neurological system properly interprets the increase of activity of the mechanoreceptors as being in response to a drop in peripheral vascular resistance and compensates by increasing the heart rate and constricting the blood vessels. However, in certain patients, as a result of a neurological condition within the vagus nerve or for some other reason, the surge in neural traffic is falsely perceived by the neurological system as being representative of hypertension. In response thereto, the brainstem triggers an increase in peripheral vasodilation and a reduction in heart rate. The vasodilation and the drop in heart rate, in turn, cause a still further reduction in blood pressure, i.e. hypotension. In other words, the actions taken by the brainstem exacerbate the problem. If the degree of hypotension is sufficiently severe, cerebral hypoperfusion occurs wherein brain cells do not receive enough oxygen and, consequently, the victim loses consciousness. Accordingly, within these patients, any sudden drop in peripheral vascular resistance can trigger vasovagal syncope and the patients are then to suffer from recurrent vasovagal syncope. Further information regarding vasovagal syncope may be found in S. Serge Harold and Jacques Mugica, Recent Advances in Cardiac Pacing, Futura Publishing Company, 92-95, 1997.
As can be appreciated, loss of consciousness can be particularly dangerous for the patient if occurring while the patient is driving a motor vehicle, climbing a flight of stairs or engaged in any other activity wherein the loss of consciousness could result in injury or death. Accordingly, it is highly desirable to provide techniques for preventing vasovagal syncope or other forms of neurocardiological syncope. One possible technique for preventing vasovagal syncope is to employ a pacemaker, or other implantable cardiac pacing device, to pace the heart to prevent the reduction in blood pressure associated with vasovagal syncope from occurring. Indeed, the American College of Cardiology-American Heart Association suggested in 1991 that vasovagal syncope in patients should be used as a Class 2 indication for pacing therapy. However, conventional cardiac pacemakers have had only limited success in preventing recurrent vasovagal syncope. (See David G. Benditt et al., Cardiac Pacing for Prevention of Recurrent Vasovagal Syncope, Ann Intern Med. 1995; 122; 204-209.)
With many conventional techniques for preventing vasovagal syncope, the cardiac pacemaker analyzes a sequence of intrinsic heart beats (i.e. natural or non-stimulated heart beats) to determine whether the sequence of heart beats indicates an episode of vasovagal syncope and, if so, the pacemaker then begins pacing the heart. In one example, if the intrinsic heart rate falls below a lower threshold, the pacemaker then analyzes the immediately preceding heartbeats to determine whether a sharp drop in heart rate has occurred. If so, the pacemaker then continues to monitor intrinsic heart beats to determine whether the heart rate remains at a stable rate below the threshold rate. If the rate remains stable for a predetermined number of heartbeats, the pacemaker then concludes that an episode of vasovagal syncope may be occurring and begins pacing at an elevated heart rate. Unfortunately, by the time the pacemaker has had the opportunity to analyze a sufficient number of heart beats to determine whether an episode of vasovagal syncope is occurring, the blood pressure of the patient has likely dropped to the point where an elevated heart rate will not remedy the vasovagal syncope and the patient will become unconscious. In this regard, the drop in blood pressure results in significantly less blood filling the ventricles, such that there is simply not enough incoming blood to pump. Hence, overall blood pressure is not significantly increased merely by pumping the heart faster, and the aforementioned cerebral hypoperfusion still occurs resulting in unconsciousness. Indeed, depending upon the programming of the pacemaker, it may take five to eight seconds or more before the pacemaker begins increasing the heart rate.
Accordingly, it would be highly desirable to provide an improved cardiac pacing device capable of promptly pacing the heart upon detection of a sudden drop in heart rate caused by vasovagal syncope or other conditions, so as to prevent a sudden drop in blood pressure to thereby more effectively prevent loss of consciousness.
In accordance with the invention, a method is provided for use in an implantable cardiac pacing device for preventing a sudden heart rate drop. With the method, an intrinsic heart rate is sensed and the heart is selectively paced while applying rate smoothing to the intrinsic ventricular rate, regardless of the intrinsic ventricular heart rate. The rate smoothing technique may also be applied to the atrial rate as well.
In an exemplary embodiment, wherein the implantable cardiac pacing device is a pacemaker or ICD, rate smoothing is applied so as to prevent a sharp heart rate increase while still permitting a sharp heart rate increase as may be required, for example, as a result of sudden exertion. This rate smoothing technique is referred to herein as a xe2x80x9cdownwardxe2x80x9d rate smoothing technique. By employing downward rate smoothing to prevent a sudden drop in heart rate, pacing can begin promptly upon detection of the drop in heart rate. This is in contrast with the conventional vasovagal syncope detection techniques discussed above wherein no pacing may occur until well after the heart rate has dropped and hence well after the blood pressure of the patient has dropped, possibly resulting in loss of consciousness. Also, by applying downward rate smoothing regardless of intrinsic ventricular heart rate, the rate smoothing prevents a sharp drop in heart rate from an otherwise normal heart rate as typically occurs during vasovagal syncope. In addition to helping to prevent vasovagal syncope, the rate smoothing technique also helps prevent long sinus pauses, which sometimes result in a malignant arrhythmia.
In a specific exemplary embodiment, the downward rate smoothing is applied during the determination of an escape interval as follows. After each newly paced or sensed heart beat, the device determines a sensor indicated rate (xe2x80x9cSIRxe2x80x9d), a base rate interval, and a measured rate interval (xe2x80x9cMRIxe2x80x9d). Then the measured rate interval is compared with a filtered rate interval (xe2x80x9cFRIxe2x80x9d) initially set to a default value. If the MRI is less than the previous FRI, then the FRI is reset to be equal to the greater of the MRI and the previous FRI, minus a decrement value. If the MRI is not less than previous FRI, then the FRI is reset to be equal to the lesser of the MRI and the previous FRI, plus an increment value. In either case, once the FRI has been reset, the escape interval is then set to the lesser of the SRI, the base rate interval and the FRI, plus a predetermined time interval. During each cycle, if a sensed beat is not detected before the escape interval elapses, a pacing pulse is applied to the heart.
This downward rate smoothing algorithm has the effect of slowing a sudden decrease in heart rate, but not impeding a sharp increase in heart rate, as may occur as a result of orthostatic stress. Hence, if the heart rate needs to increase properly as a result of sudden vigorous activity, the ventricular rate smoothing algorithm does not prevent that increase.
Apparatus embodiments of the invention are also provided. Other features, advantages and aspects of the invention are either described below or will be apparent from the descriptions below in combination with the accompanying drawings.